A further well­established effect of EDTA infusion involves the improvement of cell membrane integrity and consequent protection of mitochondria activity. If this is happening in the heart muscle itself, such improvement in cell function (enhanced energy production via enhanced mitochondria activity) often allows a strong chance of salvaging and regenerating previously damaged muscle function, with benefits to the heart and therefore the body as a whole.

Research by Dr C Gallagher as long ago as 1960 (Gallagher, 1960) showed that the natural ageing of the mitochondria could be counteracted by use of EDTA.

Not only does EDTA remove circulating ionic calcium from the blood, but it also acts directly on improving the function of blood platelets. These (which contain granules, lysosomes, mitochondria and glucose), along with red and white blood cells (erythrocytes and leucocytes), make up much of the 'solid' material suspended in the blood plasma which itself is made up of a complex of protein­based substances including fibrinogen, albumin and globulin, as well as carrying in solution salts, hormones and a variety of metabolic products and wastes.

Platelets have as a major function the role of initiating repair of any damaged internal lining in blood vessels. This they accomplish, under the direction of prostaglandin hormones called prostacyclin (which discourages clotting and reduces muscle spasm) and thromboxane (which encourages muscle spasm and the stickiness of blood), firstly by adhering to the damaged surface, gradually covering the region of injury, while at the same time reducing the danger of hemorrhage by encouraging a degree of coagulation of the blood. As all this happens, the shape of the platelets alters from a disc shape to a more irregular form, with radiating filaments known as pseudopodia extending from them as well as developing inside them. These protective functions of platelets are therefore life­enhancing. But, should the process of organization of clots (coagulation) take place in a cerebral artery the consequences could well be life­threatening and would certainly pose a hazard until it resolved.

Just how EDTA reduces these dangers is not clear, but it does. The reduction, after use of EDTA, in the tendency to overcoagulation is thought by some to relate to the way EDTA removes ionic calcium from the membrane of the platelet. Or it may be that a more healthy, balanced production of the prostaglandins which control platelet function and activity are influenced by the way EDTA inhibits lipid peroxidation, since prostoglandins are the product of lipids which can be severely damaged by free radical activity.

Normalizing abnormal cholesterol and high density lipoprotein (HDL) levels

As we age there is an increasing tendency for our bloodcholesterol levels to rise. High blood cholesterol was for many years used alone as a marker of increased risk of cardiovascular disease. The fashion for blaming all cholesterol has only partly been reduced in the public mind through education, but medical practitioners now know that it is only some forms of cholesterol which pose a real threat ­ the low density forms (LDL). Indeed the ratio between total cholesterol and HDL (high density lipoprotein beneficial form) is now used as a clear indication of relative safety or danger, in terms of being a predictor of cardiovascular disease.

In a series of simple but effective experiments, McDonagh, Rudolph, and Cheraskin (1982b) have shown that EDTA infusion has a markedly beneficial effect on this potentially serious problem.

The effects on over 200 patients with varying levels of HDL cholesterol measurements were quite dramatic. Those who initially showed low levels of HDL rose to normal levels, those with normal levels remained unaltered, and those with high levels of LDL (dangerous) dropped to normal ranges after EDTA­chelation therapy (supported with vitamin and mineral supplementation).

Thus we see a homoeostatic (balancing, normalizing) effect after the use of EDTA, since it supported a return towards normal HDL­cholesterol levels, whether the initial abnormality was high or low.

How long before such change starts to be significant?

This same team of researchers, working in a private practice setting, found that: ' . . there appears to be a significant reduction in serum cholesterol within the first month or so (range of 12­36 days) of treatment with EDTA . . . in private practice environment, irrespective of the age or sex of the patient' Excitingly, it was found that: '. . . those with the highest initial cholesterol scores decreased about twice as much as those with the lower first score (approximately 17 per cent as against 9 per cent)'

With regard to the ratios between total cholesterol and HDL, these homoeostatic effects were measured as follows:

The 'normal, balance between total cholesterol and HDL is considered to be a ratio of 4.5:1. The McDonagh, Rudolph and Cheraskin team found that those with 'relatively low ratios (under 4.0) tended to rise, while those with relatively high ratios (over 5.0) tended to decline, and those in the range 4.0­4.9 tended to remain unchanged'

This important research is deserving of far wider awareness and application since cardiovascular disease is the number one killer and these risk factors are demonstrably easy and safe to control or normalize (by EDTA, diet and life­style changes).

In Chapter 4 we looked at some of the ways in which cardiovascular disease developed. Once a localized area of plaque has accumulated in an artery, following some degree of local irritation and subsequent repair (which the plaque represents to a large extent), there exists a strong case for trying to remove any calcium in the plaque in order to prevent its inevitable build up towards this becoming a complete obstruction. It is the loosely bound calcium in the plaque, held by an electrostatic charge, which prevents the body from dissolving it. When EDTA is infused it mops up the ionic (free) calcium in the blood serum, triggering release of parathormone. This produces a demand for calcium in the blood and this is first mobilized from the calcium deposited in metastatic sites (plaque, soft tissue deposits, etc.), thus allowing the process of resorption of the plaque material and restoration of normal arterial status.

However, this does not happen quickly. It is only by repetitive, very slow infusions of EDTA that the process takes place safely

Does this not damage bone and tooth structure?

On the contrary, the status of bone is enhanced after a series of EDTA chelation infusions. This is directly related to the influence of parathyroid hormone. After EDTA infusion there is a rapid removal of ionic calcium from the bloodstream (the EDTA/calcium complex is excreted via the kidneys). The resulting drop in circulating calcium stimulates parathyroid hormone production which results in the removal of ionic calcium from metastatic deposits (such as occur in plaque). At the same time a phenomenon occurs in response to parathormone, described by Doctors Rasmussen and Bordier (1974), in which preosteoblasts are converted into osteoblasts.

Since osteoblasts are the cells which form bone, building the osseous matrix of the skeleton, new bone formation is thus encouraged. This is often confirmed by X­ray examination of bone before and after a series of chelation infusions.

According to Cranton and Brecher (1984):

Pulsed intermittent parathormone stimulation, produced by each chelation (treatment) is known to cause a lasting effect on osteoblasts of approximately three months' duration. This is a proven effect of EDTA, and one that makes perfect sense, for it provides a hypothetical explanation for the three month waiting period for complete benefit following a series of intravenous EDTA therapy infusions.

Walker and Gordon (1982) suggest that:

Soft tissue pathological calcium in plaques or arterial cells continues to diminish in order to meet the need caused by the increased bone uptake of calcium. The therapeutic cycle continues long after a series of chelation treatment has been completed and patients continue to improve all this time.

They describe the work of Dr. Carlos Lamar who explained his findings on this topic at the fourteenth annual meeting of the American College of Angiology in 1968. Dr Lamar had demonstrated that as calcification of the blood vessels decreased so did simultaneous recalcification take place of previously osteoporotic vertebral and femoral bones. Similarly, metastatic calcium deposits in arthritic joints was often seen by Dr Lamar to decrease. In such cases deformity often remained but symptoms of pain and immobility were reduced or absent after chelation therapy. Walker and Gordon remind us, however, that chelation itself is not the whole answer: 'Hardened arteries get softer and softened bones get harder following proper EDTA chelation therapy ­where appropriate mineral supplementation with zinc, magnesium and other minerals is being given, dietary calcium/phosphorus ratio is balanced and active exercise undertaken.'[original italics]

By now the concept of free radical damage resulting in tissue damage and consequent deterioration of circulatory function should be quite familiar. It is perhaps less apparent that free radical damage is frequently the trigger which leads to malignant changes in previously normal cells. Just as the first benefits to circulation of EDTA chelation therapy were discovered during treatment of heavy metal poisoning, so was the way in which this same treatment could help prevent, and indeed treat, cancer discovered.

Writing in a Swiss medical journal in 1976, Dr W Blumen described the strange but potentially very important discovery. In the late 1950s a group of residents of Zurich who lived adjacent to a major traffic route were treated for contamination by lead with EDTA chelation under the auspices of the Zurich Board of Health. These people had all inhaled large amounts of lead­laden fumes and were suffering from a range of symptoms identified as being related to lead poisoning, including stomach ache, fatigue, headache, digestive symptoms, etc. lead deposits were found to be present in their gum tissues and specific changes were found in their urine, linking their condition with high lead levels.

Some years later, in the early 1970s, people living in the same area were being investigated for the incidence of cancer, in an attempt to link the pollution with a higher cancer rate than average. This link was easily established as fully 11 per cent of the residents of the road had died of cancer over the period 1959 to 1972, a rate some 900 per cent above that expected when compared with people living in the same community but not directly affected by lead pollution. The forms of cancer most commonly related involved the lungs, colon, stomach, breast and ovary.